胰岛素样生长因子通过NF-kappaB/MuRF1通路延缓失神经骨骼肌萎缩

目的：研究胰岛素样生长因子（IGF-1）对核转录因子kappaB（nuclear factor of kappaB,NF-κB）p65活性的影响,探讨胰岛素样生长因子防治肌萎缩的作用及其机制。方法：Wistar大鼠48只,随机分为失神经对照组和实验组（药物组）,取各组不同时段腓肠肌（gastrocnemius,GAS）样本,测定肌肉萎缩程度并采用逆转录聚合酶链反应（RT-PCR）与Western Blot技术检测NF-κB mRNA和蛋白质的表达量。结果：去神经骨骼肌萎缩时,药物各组与失神经组的腓肠肌NF-κB的mRNA和蛋白质的表达在去神经支配后第2、7、14、28天同时段比较均下调,P〈0.01。结论：大鼠失神经骨骼肌萎缩早期,胰岛素样生长因子是通过NF-κB途径来防治失神经早期的骨骼肌萎缩的。

Insulin-like growth factor 1 retarding denervated skeletal muscle atrophy through inhibiting NF-kappaB/MuRF1 pathway

Objective：To study the influence of Insulin-like growth factor 1（IGF-1）on the expression pattern of nuclear factor of kappaB（NF-κB）,explored the preventive and therapeutic effect and mechanisms of Insulin-like growth factor 1 on denervated skeletal muscle atrophy.Methods：Levels of NF-kappaB p65 mRNA and protein in the gastrocnemius at different time after denervation were detected respectively by RT-polymerase chain reaction（RT-PCR）and Western Bloting.The ratio of muscle wet weight was also analyzed for comparison.Results：The effect showed that only the expression of NF-κB mRNA and protein level in specimens of Insulin-like growth factor 1 group were down-regulated at 2,7,14,28 days after denervation,compared with denervation group（P〈0.01）.Conclusion：NF-κB expression of gastrocnemius denervation model of rats can be down-regulated by Insulin-like growth factor 1,which shows that Insulin-like growth factor 1 is a effective way of delaying denervated skeletal muscle atrophy through participate in NF-κB path.